Characteristics of atopic dermatitis include 1) altered reactivity to cholinergic and other pharmacologic agents, 2) elevated serum IgE and 3) diminished cell mediated immunity (CMI). Previous studies have indicated subnormal cyclic AMP responses in atopic lymphocytes stimulated by beta-adrenergic agents in vitro. Recent findings in this laboratory indicate IgE binding to lymphocytes and functional impairment of lymphocytes in vitro. We propose that IgE bound to the lymphocyte membrane may be responsible for the alterations in cellular immunity and pharmacologic responsiveness. We intend to evaluate a) the nature and extent of IgE binding to lymphocytes; highly purified cells will be assessed for specificity of binding to various subpopulations and for conditions which enhance or inhibit binding. b) IgE influences on lymphocyte function; assays for protein and DNA synthesis and for elaboration of lymphokines will compare IgE treated and untreated lymphocytes in order to detect inhibitory effects, stimulatory activity or modification of pharmcologic responsiveness. c) In vivo models of atopic dermatitis; substances released from stimulated lymphocytes will be tested for capacity to reproduce atopic dermatitis lesions in normal and atopic dogs.